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Beck Depression Inventory GSK study Dyskinesia in Parkinson's disease NCT00363727

- 9/8/17 - 1 form, 2 itemgroups, 4 items, 1 language
Itemgroups: General information, Beck Depression Inventory
Study ID: 101468/228 Clinical Study ID: 101468/228 Study Title:A two year Phase IIIb randomised, multicenter, double-blind, SINEMET controlled, parallel group, flexible dose study, to assess the effectiveness of controlled release ropinirole add-on therapy to L-dopa at increasing the time to onset of dyskinesia in Parkinson's disease subjects. Patient Level Data: Study Listed on ClinicalStudyDataRequest.com Clinicaltrials.gov Identifier: NCT00363727 Sponsor: GlaxoSmithKline Collaborators: N/A Phase: phase 3 Study Recruitment Status: Completed Generic Name: ropinirole Trade Name: Zygara,ZIPEREVE,ZEPREVE,Requip Depot,REQUIP,REPREVE,Modutab,ADARTREL Study Indication : Dyskinesias; Parkinson Disease; Parkinson's Disease Study part: Beck Depression Inventory.

dbGaP phs001071 NINDS Family-Based Whole-Genome Sequencing to Find HD Modifiers - pht005344.v1.p1

- 6/23/23 - 6 forms, 1 itemgroup, 3 items, 1 language
Itemgroup: pht005344
Principal Investigator: Steven Finkbeiner, Gladstone Institutes, San Francesco, CA, USA MeSH: Huntington Disease,Degenerative Hereditary Diseases, Nervous System,Cell Death,Brain Diseases,Ataxia,Chorea,Cognition Disorders,Dyskinesias,Mental Disorders https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001071 The goal of our studies is to identify genetic modifiers of neurodegeneration in Huntington's disease (HD). HD is caused by expansion of CAG repeats in the huntingtin (Htt) gene, with longer stretches often leading to more rapid disease onset and progression. Yet, for a given number of repeats, the age of symptom onset can be variable, differing by up to decades. Thus, the age of onset of motor symptoms in HD is only partly explained by the length of the CAG expansion. Available evidence suggests that genetic modifiers contribute to the variation in HD onset. Identifying genetic modifiers is important because they may provide critical insights into HD pathogenesis and reveal key pathways that could be targeted by novel HD therapeutics. This is important since there are no disease-modifying therapies for HD, and mHtt is an unattractive small-molecule drug target. We recruited 21 HD families with varying characteristics of disease progression and age of onset and obtained medical histories, clinical records and DNA samples that were subjected to whole-genome sequencing (WGS). These WGS data describe families of 104 subjects, including HD patients and their unaffected family members. These individuals were selected based on individual clinical histories and family structures that best fit our criteria for expressing potential genetic modifiers. We are testing the hypothesis that novel, rare genetic variants contribute to HD and those genetic modifiers can be identified by WGS.

pht005345.v1.p1

1 itemgroup 5 items

pht005346.v1.p1

1 itemgroup 3 items

pht005347.v1.p1

1 itemgroup 8 items

pht005348.v1.p1

1 itemgroup 4 items

Eligibility

1 itemgroup 6 items

Neurological examination GSK study Dyskinesia in Parkinson's disease NCT00363727

- 9/7/17 - 1 form, 2 itemgroups, 20 items, 1 language
Itemgroups: General information, Neurological examination
A two year Phase IIIb randomised, multicenter, double-blind, SINEMET controlled, parallel group, flexible dose study, to assess the effectiveness of controlled release ropinirole add-on therapy to L-dopa at increasing the time to onset of dyskinesia in Parkinson's disease subjects. Patient Level Data: Study Listed on ClinicalStudyDataRequest.com Clinicaltrials.gov Identifier: NCT00363727 Sponsor: GlaxoSmithKline Study part: Neurological examination

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